戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 owed significantly reduced expression of the chemokine CCL2.
2 type I interferon-mediated production of the chemokine CCL2.
3 -beta and the peripheral induction of the CC chemokine CCL2.
4  T cells and partially requires the secreted chemokine CCL2.
5 itment in vivo by inducing expression of the chemokine CCL2.
6  enhanced renal expression of the macrophage chemokine CCL2.
7 quency and upregulates the expression of the chemokine CCL2.
8 nce of increased expression of the mast cell chemokine Ccl2.
9  manifest increased expression levels of the chemokine Ccl2.
10 learance, due to decreased production of the chemokine CCL2.
11 sion molecule E-selectin or secretion of the chemokine CCL2.
12 he islets is caused by overexpression of the chemokine CCL2.
13 ton and cell polarization in response to the chemokine CCL2.
14 biological properties of the prototypical CC chemokine, CCL2.
15 orresponds to the levels of its ligands, the chemokines Ccl2, 7, and 8.
16          The initial cellular sources of the chemokine CCL2, a ligand for CCR2, included perivascular
17 mutants also induced increased levels of the chemokine CCL2, a monocyte chemoattractant, in serum, an
18 ons was coupled with lack of upregulation of chemokine CCL2 after nerve injury and reduced accumulati
19 udies in mice that implicated a role for the chemokine CCL2 (also known as MCP1) and macrophages.
20  usually characterized by high levels of the chemokine CCL2 and a prodigious monocyte/macrophage infi
21            The Slc35c1 cKO increased hepatic chemokine Ccl2 and Cxcl2 expression and T cell, neutroph
22 omous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony-stimula
23 ection and correlated to increased levels of chemokine CCL2 and greater neutrophil recruitment.
24 e substantial amounts of the proinflammatory chemokine CCL2 and immunosuppressive cytokine IL-10, in
25                                          The chemokine CCL2 and its primary receptor CCR2 are key reg
26                We show that the inflammatory chemokine CCL2 and its receptor CCR2 are necessary for t
27 pression of multiple pathways, including the chemokine CCL2 and its receptor, CCR2.
28                     Marked reductions in the chemokine Ccl2 and the pro-inflammatory cytokine Tnfalph
29 (+) and CD8(+) T cells, upregulation of beta-chemokines (CCL2 and CCL22), basic fibroblast growth fac
30              Therefore, drugs targeting beta-chemokines (CCL2 and CCL22), FGF-basic, HGF, or MIF migh
31  Although STAT3 inhibition downregulated the chemokines CCL2 and CCL12, which can signal through CCR2
32 the migration of macrophages directed by the chemokines CCL2 and CCL19, activation of the actin-remod
33 nd TNF-alpha, as well as the proinflammatory chemokines CCL2 and CCL3, and chemokine receptors CCR1 a
34 f the CXCL1 dimer is novel: dimers of the CC chemokines CCL2 and CCL4 are inactive, and the dimer of
35  expression of mRNAs for the proinflammatory chemokines CCL2 and CCL5 than mock- and E3 null virus-in
36 LTalpha1beta2 also induced production of the chemokines CCL2 and CCL5, which elicited transmigration
37 erred enhanced expression of proinflammatory chemokines CCL2 and CCL5.
38 ed by elevated levels of monocyte-recruiting chemokines CCL2 and CCL7 and infiltration of CCR2(+)Ly6C
39                                          The chemokines CCL2 and CCL7 are upregulated in the brain du
40 igand treatment, decreased expression of the chemokines CCL2 and CCL7 by astrocytes in EAE.
41 d TNF-alpha each stimulate production of the chemokines CCL2 and CCL7 in astrocytes in a concentratio
42  signaling pathway induced the expression of chemokines CCL2 and CCL7 in colorectal tumor cells, lead
43 e relative contribution of the CCR2 ligands, chemokines CCL2 and CCL7, in directing monocyte mobiliza
44 C) subtypes heightened the expression of the chemokines CCL2 and CCL7, supporting the homing of CCR2(
45 ll as a reduction in the monocyte-recruiting chemokines CCL2 and CCL7.
46 at intercellular adhesion molecule-1 and the chemokines CCL2 and CX3CL1 probably are involved in leuk
47 a was associated with greater release of the chemokines CCL2 and CXCL12, the cytokines interleukin-6
48 iments revealed MC-derived expression of the chemokines CCL2 and MIF, which actively preserved macrop
49   Of interest, we found that expression of 2 chemokines, CCL2 and CXCL10, correlated with the median
50 hese observations by demonstrating that MPhi chemokine (CCL2) and receptor (CCR2) knockout mice displ
51 e resulting products by Nod2, release of the chemokine CCL2, and CCR2-dependent recruitment of the ad
52 ukin-1beta, tumor necrosis factor-alpha, the chemokine CCL2, and interferon regulatory factor-5 (IRF5
53 infiltration into tissues in response to the chemokine CCL2, and, like atypical chemokine receptors (
54 k in our laboratory has shown a role for the chemokine, CCL2, and its receptor in the induction of hi
55 xpressed the T-cell- and monocyte-attracting chemokine, CCL2, and the T-cell-supporting cytokine, IL-
56 and IL-13-treated fibroblasts; we identified chemokine CCL2 as a potential target.
57 ocytes, which express CCR2 (the receptor for chemokine CCL2), as well as the subsequent recruitment o
58 re model of the human BBB in response to the chemokine CCL2, as well as in disruption of the BBB, as
59 d Schu S4 did not stimulate secretion of the chemokine CCL2 by HUVECs, whereas material released from
60  HIF1alpha, which increased secretion of the chemokine CCL2 by tumor cells and promoted recruitment o
61 A treatment also reduced the MDSC-attracting chemokine CCL2 (C-C motif ligand 2) in the TME along wit
62  New work showing that the T cell-attracting chemokine CCL2 can be posttranslationally modified in th
63 ha, IL-1beta, IL-6, IL-12, G-CSF and GM-CSF, chemokines-CCL2, CCL11, CXCL1, CXCL8 and CXCL10, acute p
64 d with decreased expression of M2-associated chemokines (CCL2, CCL3, and CXCL2) and cytokines (IL6, I
65                              A subset of six chemokines (CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL10) w
66                                          Six chemokines (CCL2, CCL3, CCL4, CXCL8, CXCL10 and CX3CL1)
67                                          Six chemokines (CCL2, CCL3, CCL4, CXCL8, CXCL10, and CX3CL1)
68 ably, cytokines IL-6, TNF, and IFN-gamma and chemokines CCL2, CCL3, and CCL4 have been associated wit
69 croglial activation marker Iba1 and CC motif chemokines CCL2, CCL3, and CCL5.
70 roduction in the lung of the proinflammatory chemokines CCL2, CCL3, CCL5, CXCL9, and CXCL10 with diff
71 ponse genes STAT1, STAT2, Mx1, OASL2, ISG15, chemokines CCL2, CCL3, CXCL9 and CXCL10, and the frequen
72 ic subsets of cytokines (TNFalpha, IL-6) and chemokines (CCL2, CCL4, CXCL1, CXCL2, CXCL10) are critic
73 eta, interleukin 12, and interleukin 17; the chemokines CCL2, CCL4, and CXCL10; and the growth factor
74 L-1beta), interleukin 18, and interleukin 6; chemokines CCL2, CCL4, CCL11, CCL22, CXCL8, and CXCL10;
75 e that H. pylori increases production of the chemokines CCL2, CCL5, and granulocyte-macrophage colony
76                                    mRNAs for chemokines CCL2, CCL5, CCL17, IFN-gamma inducible chemok
77  fibroblast growth factor 2 (FGF-2), and the chemokines CCL2, CCL5, CCL7, CCL13, CXCL8, and CXCL10 we
78 kaged in ESTA-MSV efficiently suppressed the chemokines, CCL2, CCL5, CCL8, and CXCL9, and monocyte ad
79 and (CXCL) 1 chemokines and up-regulation of chemokine (Ccl2, Ccl7, Cxcl1, Cxcl2, and Cxcl10) and cel
80 IFN-I signaling stimulated the production of chemokines (CCL2, CCL7, and CCL12) that recruited Ly6C(h
81 tokines (TNF-alpha, IL-1beta, IFN-gamma) and chemokines (CCL2, CCL8, and CCL5) and an increase in adi
82 L-1A, IL-1B, IL-23A, IL-17C, and IL-32), and chemokines (CCL2, CCL8, and CXCL5).
83                                          The chemokines CCL2, CCL8, CXCL1, and CXCL2 ranked highest a
84                  Finally, nociceptor-derived chemokine CCL2 contributes to the orchestration of DC-de
85 nt inhibitor (ICI) via secretion of numerous chemokines (Ccl2, Cx3cl1, and Tgf-B1), which recruit imm
86 matory cytokines (Il1b, Il23, Tgfb1, Il17a), chemokines (Ccl2, Cxcl1, Cx3cl1) and chemokine receptors
87 or alpha [TNFalpha], interleukin [IL]-6) and chemokines (CCL2, CXCL2) were also significantly lower i
88 ies reveal that interleukins (IL-1a, IL-1b), chemokines (CCL2, CXCL8), and TNF-alpha, are all signifi
89 ptionally high levels of IFN-gamma-inducible chemokines, CCL2, CXCL9, and CXCL10; and this pronounced
90 ovascular endothelial cells (BMECs) with the chemokine CCL2 (formerly called MCP-1).
91 n IL-1beta-deficient mice, low levels of the chemokine CCL2 hamper recruitment of monocytes and, toge
92                                          The chemokine, CCL2, has been shown to play a major role in
93 vels of pro- and anti-inflammatory cytokines/chemokines (CCL2, IL-6, CXCL2, KC, TNF-alpha, and IL-10)
94 sion programs, and the level of the monocyte chemokine CCL2 in bronchoalveolar lavage fluid positivel
95 tween RNS-modified tyrosine residues and the chemokine CCL2 in diseased kidneys.
96 ntified a microRNA-regulated pathway for the chemokine CCL2 in HCV-induced hepatitis.
97 ociated with increased concentrations of the chemokine CCL2 in lung lavage.
98 dependent) upregulation of expression of the chemokine CCL2 in mast cells.
99                  Increased expression of the chemokine CCL2 in the CNS has been demonstrated to be im
100   The present study examined the role of the chemokine CCL2 in the control of Salmonella infection.
101 mmatory genes, including monocyte/macrophage chemokine Ccl2, in Pik3caH1047R-iLECs was associated wit
102 ent study dissects the mechanisms by which a chemokine, CCL2, induces TJ disassembly.
103                                          The chemokine CCL2, intended to attract monocyte-macrophage
104                                          The chemokine CCL2 is one of the most elevated inflammatory
105                                 However, the chemokine CCL2 is significantly expressed in the DRG of
106 though recent studies have suggested that CC chemokine CCL2 may directly affect the angiogenesis, the
107 ation-induced increases in mRNA encoding the chemokine CCL2 (MCP-1) and release of the protein.
108 IFN-gamma) and tumor necrosis factor and the chemokine CCL2 (MCP-1) were seen after infection of susc
109 ly decreases expression and secretion of the chemokine CCL2 (MCP-1).
110 s B4 and C4, the cytokines IL-6 and TNF, and chemokines CCL2 (MCP-1) and CCL4 (MIP-1beta).
111  dramatic reduction in the production of the chemokines CCL2 (MCP-1) and CXLC2 (MIP-2) in TNFR1-defic
112 lation, such as heightened expression of the chemokines CCL2 (MCP-1), CCL3 (MIP-1alpha), CCL4 (MIP-1b
113                      Moreover, expression of chemokine CCL2, MCP-1 and its receptor CCR2, which play
114            Cytokine array indicated that the chemokine CCL2/MCP-1 (monocyte chemoattractant protein-1
115                                              Chemokine CCL2/MCP-1 is known to attract CCR2(+) monocyt
116 in a marked increase in SMC secretion of the chemokine CCL2/MCP-1, which has been previously shown to
117 d IL-6, and markedly enhanced secretion of a chemokine, CCL2/MCP-1, important modulators of inflammat
118  this study, we identified four inflammatory chemokines (Ccl2/Mcp-1, Ccl7, Cxcl16, and Cx3cl1) of ove
119  necrosis factor-alpha, IL-6, and IL-1beta), chemokines (CCL2/MCP-1, CXCL1/GROalpha, CXCL3/GROgamma,
120 ular mechanism by which the pro-inflammatory chemokine CCL2 mediates brain endothelial barrier disrup
121 kines (IL-1 beta, TNF-alpha, and S100B), the chemokine CCL2, microglial activation, seizure susceptib
122 timulated HUVEC, and the endothelium-derived chemokine CCL2 (monocyte chemoattractant protein 1) was
123 a recombinant coronavirus that expressed the chemokine CCL2/monocyte chemoattractant protein-1.
124 ) were found to be the most abundant, but CC chemokines (CCL2/monocyte chemotactic protein 1 and CCL3
125                The neuroinflammatory markers chemokine CCL2, NF-kappaB and nitrotyrosine were localiz
126 ired the chemokine receptor CCR2 but not the chemokine CCL2 or receptor CCR7.
127  (IL)-6, IL-8, and IL-13, and lower monocyte chemokine, CCL2 (P < .01 for each).
128 cible skin signature wherein the profibrotic chemokine CCL2 plays a key role.
129 n, leukotriene C(4) (LTC(4)) generation, and chemokine CCL2 production.
130 F-induced LTC(4) generation, is required for chemokine CCL2 production.
131                                          The chemokine CCL2 promotes kidney disease in two models of
132           We also show that the inflammatory chemokine, CCL2, protects against tat toxicity and inhib
133                        Neutralization of the chemokine CCL2 reduced cancer-associated pain in a clini
134 wth factor, transforming growth factor beta, chemokine CCL2, SDF-1, and complements C3, C4, and facto
135 ecrosis factor-alpha, interleukin-6, and the chemokine CCL2, than CD11b(+)Gr-1(+) cells isolated from
136          Prefrontal cortex expression of the chemokine Ccl2 was increased acutely, while small intest
137  430, and the effects on serum levels of the chemokine CCL2 were measured 4 h later.
138  macrophages, inducing the production of the chemokine CCL2, which in turn recruited circulating CCR2
139 ted that macrophages and the inflammatory CC-chemokine CCL2, which is scavenged by ACKR2, are associa
140 e I IFN response inhibited production of the chemokine CCL2, which promotes the recruitment of macrop
141 loss of Mir155 reduced the expression of the chemokine CCL2, which promotes the recruitment of monocy
142 cells leads to an increased secretion of the chemokine CCL2, which recruits IBA1-expressing myeloid c
143 mice exhibited increased serum levels of the chemokine CCL2, which resulted in the recruitment of bot

 
Page Top